ABSTRACT: BACKGROUND: The purpose of this study was to examine the efficacy of 15 days of betaine supplementation on muscle endurance, power performance and rate of fatigue in active college-aged men. METHODS: Twenty-four male subjects were randomly assigned to one of two groups. The first group (BET; 20.4 +/- 1.3 years; height: 176.8 +/- 6.6 cm; body mass: 77.8 +/- 13.4 kg) consumed the supplement daily, and the second group (PL; 21.4 +/- 4.7 years; height: 181.3 +/- 5.9 cm; body mass: 83.3 +/- 5.2 kg) consumed a placebo. Subjects were tested prior to the onset of supplementation (T1) and 7 (T2) and 14 days (T3) following supplementation. Each testing period occurred over a 2-day period. During day one of testing subjects performed a vertical jump power (VJP) and a bench press throw (BPT) power test. In addition, subjects were required to perform as many repetitions as possible with 75% of their 1-RM in both the squat and bench press exercises. Both peak and mean power was assessed on each repetition. On day two of testing subjects performed two 30-sec Wingate anaerobic power tests (WAnT), each test separated by a 5-min active rest. RESULTS: No differences were seen at T2 or T3 in the repetitions performed to exhaustion or in the number of repetitions performed at 90% of both peak and mean power between the groups in the bench press exercise. The number of repetitions performed in the squat exercise for BET was significantly greater (p < 0.05) than that seen for PL at T2. The number of repetitions performed at 90% or greater of peak power in the squat exercise was significantly greater for BET at both T2 and T3 than PL. No differences in any power assessment (VJP, BPT, WAnT) was seen between the groups CONCLUSION: Two-weeks of betaine supplementation in active, college males appeared to improve muscle endurance of the squat exercise, and increase the quality of repetitions performed.

PMID: 19250531

Technologies for the control of fat and lean deposition in livestock.

Abstract

When the ratio of lean to fat deposition is improved, so is feed conversion efficiency. Net benefits may include lower production costs, better product quality, less excretion of nitrogenous wastes into the environment, decreased grazing pressure on fragile landscapes, and reduced pressure on world feed supplies. However, finding a way to achieve these goals that is reliable, affordable, and acceptable to the majority of consumers has proved to be a major challenge. Since the European Union banned hormonal growth promoters (HGPs) 15 years ago, countries such as Australia and the United States have licensed new products for livestock production, including bovine growth hormone (GH), porcine and equine GH, and the beta-agonist ractopamine. There has also been considerable research into refining these products, as well as developing new technologies. Opportunities to improve beta-agonists include lessening their effects on meat toughness, reducing adverse effects on treated animals, and prolonging their duration of action. In the last regard, the combined use of a beta-agonist with GH, which upregulates beta-adrenoceptors, can produce an outstanding improvement in carcass composition and feed efficiency. Insulin-like growth factor-1 (IGF-1) mediates many of the actions of GH, but has proved to be of more use as a growth reporter/selection marker in pigs, than as a viable treatment. However, a niche for this product could exist in the manipulation of neonatal growth, causing a life-long change in lean:fat ratio. Another significant advance in endocrinology is the discovery of hormones secreted by muscle and fat cells, that regulate feed intake, energy metabolism, and body composition. Leptin, adiponectin and myostatin were discovered through the study of genetically obese, or double-muscled animals. Through genetic manipulation, there is potential to exploit these findings in a range of livestock species, although the production of transgenic animals is still hampered by the poor level of control over gene expression, and faces an uphill battle over consumer acceptance. There are several alternatives to HGPs and transgenics, that are more likely to gain world-wide acceptance. Genetic selection can be enhanced by using markers for polymorphic genes that control fat and lean, such as thyroglobulin, or the callipyge gene. Feed additives of natural origin, such as betaine, chromium and conjugated linoleic acid, can improve the fat:lean ratio under specific circumstances. Additionally, 'production vaccines' have been developed, which alter the neuro-endocrine system by causing an auto-immune response. Thus, antibodies have been used to neutralise growth-limiting factors, prolong the half-life of anabolic hormones, or activate hormone receptors directly. Unfortunately, none of these technologies is sufficiently well advanced yet to rival the use of exogenous HGPs in terms of efficacy and reliability. Therefore, further research is needed to find ways to control fat and lean deposition with due consideration of industry needs, animal welfare and consumer requirements.

Effect of dietary betaine on nutrient utilization and partitioning in the young growing feed-restricted pig.

Abstract

The purpose of this study was to examine the effects of dietary betaine over a range of concentrations (between 0 and 0.5%) on growth and body composition in young feed-restricted pigs. Betaine is associated with decreased lipid deposition and altered protein utilization in finishing pigs, and it has been suggested that the positive effects of betaine on growth and carcass composition may be greater in energy-restricted pigs. Thirty-two barrows (36 kg, n = 8 pigs per group) were restrictively fed one of four corn-soybean meal-skim milk based diets (18.6% crude protein, 3.23 Mcal ME/kg) and supplemented with 0, 0.125, 0.25, or 0.5% betaine. Feed allotment was adjusted weekly according to BW, such that average feed intake was approximately 1.7 kg for all groups. At 64 kg, pigs were slaughtered and visceral tissue was removed and weighed. Carcasses were chilled for 24 h to obtain carcass measurements. Subsequently, one-half of each carcass and whole visceral tissue were ground for chemical analysis. Linear regression analysis indicated that, as betaine content of the diet was elevated from 0 to 0.5%, carcass fat concentration (P = 0.06), P3 fat depth (P = 0.14) and viscera weight (P = 0.129) were decreased, whereas total carcass protein (P = 0.124), protein deposition rate (P = 0.98), and lean gain efficiency (P = 0.115) were increased. The greatest differences over control pigs were observed in pigs consuming 0.5% betaine, where carcass fat concentration and P3 fat depth were decreased by 10 and 26%, respectively. Other fat depth measurements were not different (P > 0.15) from those of control pigs. In addition, pigs consuming the highest betaine level had a 19% increase in the carcass protein:fat ratio, 23% higher carcass protein deposition rate, and a 24% increase in lean gain efficiency compared with controls. Dietary betaine had no effects (P > 0.15) on growth performance, visceral tissue chemical composition, carcass fat deposition rate, visceral fat and protein deposition rates, or serum urea and ammonia concentrations. These data suggest that betaine alters nutrient partitioning such that carcass protein deposition is enhanced at the expense of carcass fat and in part, visceral tissue.

PMID: 11881930

Effect of betaine supplementation on plasma nitrate/nitrite in exercise-trained men.

Abstract

ABSTRACT:BACKGROUND:

Betaine, beetroot juice, and supplemental nitrate have recently been reported to improve certain aspects of exercise performance, which may be mechanistically linked to increased nitric oxide. The purpose of the present study was to investigate the effect of betaine supplementation on plasma nitrate/nitrite, a surrogate marker or nitric oxide, in exercise-trained men.METHODS:

We used three different study designs (acute intake of betaine at 1.25 and 5.00 grams, chronic intake of betaine at 2.5 grams per day for 14 days, and chronic [6 grams of betaine per day for 7 days] followed by acute intake [6 grams]), all involving exercise-trained men, to investigate the effects of orally ingested betaine on plasma nitrate/nitrite. Blood samples were collected before and at 30, 60, 90, and 120 min after ingestion of 1.25 and 5.00 grams of betaine (Study 1); before and after 14 days of betaine supplementation at a dosage of 2.5 grams (Study 2); and before and after 7 days of betaine supplementation at a dosage of 6 grams, followed by acute ingestion of 6 grams and blood measures at 30 and 60 min post ingestion (Study 3).RESULTS:

Our data indicate that acute or chronic ingestion of betaine by healthy, exercise-trained men does not impact plasma nitrate/nitrite. These findings suggest that other mechanisms aside from increasing circulating nitric oxide are likely responsible for any performance enhancing effect of betaine supplementation.

PMID:21414230

"The only good is knowledge and the only evil is ignorance." - Socrates

From what I have been reading it appears this pathway is responsible for the formation of dopamine and norepinepherine plus the formation of H²S, which allow for greater NMDA receptor activity, greater NO activity and ultimately greater initiation of steroidogenesis. SAM-e also exerts strong effects on increasing Hydrogen Sulfide (H²S) Production, which increases NMDA receptor activity.

Betaine, ATP, and SAM-e directly function within the SAM-e pathway and appears to add to product effectiveness. Betaine has also been shown to have the ability to form sarcosine (an NMDA receptor co-agonist) and act as a methyl donor to fuel SAM-e formation. Betaine donates a methyl group during the formation of SAM-e, and becomes DMG (N-N-dimethylglycine). Then the donated methyl group can then form SAM-e, or be used for the production of neurotransmitters, the production of DNA, or the metabolism of fats. The remaining DMG is then converted readily by the liver to the NR-1 agonist N-Methyl Glycine via glycine N-methyltransferase.

Possibly a combo of DAA and betaine be beneficial? Maybe I can get Dirk to comment on why he included betaine as part of the formula in Lit-Up

"The only good is knowledge and the only evil is ignorance." - Socrates

From what I have been reading it appears this pathway is responsible for the formation of dopamine and norepinepherine plus the formation of H²S, which allow for greater NMDA receptor activity, greater NO activity and ultimately greater initiation of steroidogenesis. SAM-e also exerts strong effects on increasing Hydrogen Sulfide (H²S) Production, which increases NMDA receptor activity.

Betaine, ATP, and SAM-e directly function within the SAM-e pathway and appears to add to product effectiveness. Betaine has also been shown to have the ability to form sarcosine (an NMDA receptor co-agonist) and act as a methyl donor to fuel SAM-e formation. Betaine donates a methyl group during the formation of SAM-e, and becomes DMG (N-N-dimethylglycine). Then the donated methyl group can then form SAM-e, or be used for the production of neurotransmitters, the production of DNA, or the metabolism of fats. The remaining DMG is then converted readily by the liver to the NR-1 agonist N-Methyl Glycine via glycine N-methyltransferase.

Possibly a combo of DAA and betaine be beneficial? Maybe I can get Dirk to comment on why he included betaine as part of the formula in Lit-Up

Couldnt DMG act sort of like Sarcosine and help DAA be absorbed better or am i way off here?

Couldnt DMG act sort of like Sarcosine and help DAA be absorbed better or am i way off here?

Absolutely- TMG is n-n-n methylglycine, DMG is n-n methylglycine, and Sarcosine is n-methylglycine- each time an n- is removed from the process, it acts as a methylating agent- so sarcosine is DMG with a methyl removed, just like DMG is TMG with a methyl removed

This is from the LU tech write-up: The NMDA receptor is fairly complex, in that it requires multiple stimuli, called ligands, which are molecules that act as a trigger on a target receptor to activate a biological process (discussed below). There are two crucial binding sites on NMDA receptors- the NMDA binding site (NR-2), and the glycine binding site (NR-1). The ligand with the strongest affinity (ability to bind to) for the NMDA binding site in the hypothalamus is D-Aspartic Acid, while the ligand with the strongest affinity for the glycine binding site is n-methyl glycine (also known as sarcosine), closely followed by L-Glycine, which is an amino acid. So, in review, the ligand with the strongest ability to bind the NMDA binding site (NR-2) in the hypothalamus, while the ligand with the strongest ability to bind the glycine binding site (NR-1) is n-methyl glycine (1-3,5).

This is important because the type of ligand that binds to the NR-1 binding site determines the response of the receptor. L-Glycine binds to the site quite well, but is rapidly removed from the binding site by glycine transporter 1 (GT1), a transport protein that regulates the re-uptake of glycine from the synapse (the space between nerve cells). GT1 determines the amount of glycine present between nerve endings; greater GT1 activity allows for less glycine buildup in the synapse, and the more glycine that is removed from the synapse, the less effective it can be as a co-agonist in activating the NMDA receptor. Since NMDA reception must be co-activated by two separate ligands, if one is ineffective or removed too quickly there will be little or no activation occurring, which would lead to a less effective product (7-8, 17).
 Therefore, the challenge is to isolate other ligands that can bind the GT1 and block or slow the action of the protein. Blocking or slowing the action of GT1 can allow greater amounts of glycine to build up in the synapse, which will allow greater stimulation of the NR-1 binding site. This, along with the coupling of DAA to the NR-2 binding site, is essential for attaining optimal activation of the NMDA receptor. D-Serine, D-Alanine, D-Cycloserine, and Sarcosine (N-Methyl Glycine) are compounds that have potential, in that each of these compounds can act as a ligand of the NR-1 binding site. N-Methyl Glycine is most likely the best choice in this situation, in that it limits GT1 action, thus limiting the removal of glycine from the synapse, and also because it is a ligand/co-agonist of the NR-1 binding site. This means that N-Methyl Glycine can also act on the NR-1 glycine receptor as well as GT1, making it a very effective co-agonist to the NMDA receptor. When both NR-1 and NR-2 have been successfully bound with low GT1 activity, optimal stimulation of the NMDA receptor can occur, allowing for a maximal physiological response and optimal product effectiveness (5,7-8,16).
 However, yet another compound, N,N,N-trimethylglycine (TMG) serves a multi-faceted function in a similar way to N-Methyl Glycine, D-Alanine, and D-Serine. TMG can be directly converted by the liver to the NR-1 agonist N-Methyl Glycine, which means that Lit-Up™effectively allows for a the co-agonist of the NMDA receptor to be present. However, it must first undergo a simple enzymatic conversion, which is accomplished by acting as a methyl donor. (See Figure 4 below). This means that it donates extra methyl groups to other molecules, via the methylation pathway (which enhances product quality) because the methylation pathway is responsible for the production of neurotransmitters, the structure and function of DNA, and the metabolism of fats. The conversion of TMG to N-Methyl Glycine is very efficient, therefore giving the Lit-Up™formulation excellent co-ligand enhancement for the NMDA receptor to work in conjunction with the D-Aspartic Acid. TMG has also been shown in recent human studies to have the ability to increase creatine storage within muscle cells (1-5, 16-17,61-63).
 When the NMDA binding sites are triggered in the hypothalamus by DAA and its co-agonist (in this case N-Methyl Glycine), there is an increase in cyclic guanosine monophosphate (cGMP) activity in the pituitary. cGMP is classified as a second messenger, meaning that it exerts its effects by acting in a manner secondary and in response to a first messenger signaling molecule. When the first messenger signaling molecules bind to a receptor (in this case, D-Aspartic Acid and its co-agonist bind to NR-1 and NR-2), the secondary pathway is activated that increases cGMP production. The heightened levels of cGMP in the pituitary correspond to an increased production of gonadotropin releasing hormone (GnRH), and growth hormone releasing hormone (GHRH). The resulting increase in GHRH from stimulation of the NMDA receptor also allows increased amounts of growth hormone (GH) to be secreted from the pituitary, while an increase in GnRH subsequently signals the pituitary to release luteinizing hormone (LH), and follicle stimulating hormone (FSH) (see figure 2). This increase in LH and FSH allows for an increase in steroidogenesis in the testes, which subsequently allows for the production of increased amounts of testosterone, as explained below ((1-3,10-13,43,45,59-60,75-77)

Wow, did not know betain was the same as TMG. TMG is supposed to be good stuff, but i didnt notice a difference after running it for a while so i quit. To be fair, i didnt notice anything from same-e at moderate doses either.

Never really looked into it too much and not near the depth that you provided. I'm going to have to give this a another look and dig into those studies as soon as I have some more time. I love SAM-e however, just wished it was cheaper.

Originally Posted by JudoJosh

Just got my bulk betaine in and am about to start adding a gram of it to my daily lit-up serving..

On a side note along with my betaine I got me a copy of "Anabolic Pharmacology" by Seth Roberts! Have you gotten a chance to give this a look through yet Travis?

How is it in comparison to Anaboics 9th edition? Or is that too far off to really compare? I don't know much about that one.

I have been taking 3g daily (including the amount that is in my Lit-Up which I also take daily)

Originally Posted by tnubs

Wow, did not know betain was the same as TMG. TMG is supposed to be good stuff, but i didnt notice a difference after running it for a while so i quit. To be fair, i didnt notice anything from same-e at moderate doses either.

How much were you using?

"The only good is knowledge and the only evil is ignorance." - Socrates